SARS STOCKS

[Rocketred]

April 28, 2003 / Vol. 161 No. 16
Health
Why Viruses are Hard to Kill
The latest SARS science
BY BRYAN WALSH / HONG KONG




Regional Affair: Beijing waffles as SARS strikes the interior

Essay: Where the scrubbing never stops

Cover-up: Silent for too long



MORE STORIES
Shanghai SARS Cases 'Secret'
Viruses: Hard to Kill
Hong Kong: Keep on Scrubbing
China: SARS Hits the Hinterland
Coverup: Silent for Too Long
Beijing Hoodwinks WHO Inspectors
Stalking a Killer
What are Superspreaders?
Unmasking a Crisis

PHOTOS & GRAPHICS

On Assignment: The SARS Outbreak



How the Virus Spreads



How a Coronavirus Works



How to Protect Yourself





Dr. Julie Gerberding, director of the U.S. Centers for Disease Control and Prevention, was elated. In a matter of weeks--not months or years--teams of scientists whose work was coordinated by the World Health Organization had managed to decode the entire genetic sequence of the new coronavirus now conclusively believed to cause SARS, or severe acute respiratory syndrome. "It's a scientific achievement that I don't think has ever been paralleled in human history," said Dr. Gerberding shortly before the April 16 announcement that the coronavirus's genetic fingerprint had been fully identified.

Theoretically, the achievement should lead to better diagnostic tools, treatments and perhaps even a vaccine for SARS. Germany's Artus Biotech has already released what it claims is a highly accurate test kit that can detect SARS in less than three hours. But as has been shown in AIDS research, knowing your enemy is merely the first battle in what is likely to be a lengthy war. AIDS and SARS (and the common cold, for that matter) are caused by viruses--and viruses are notoriously hard to kill. Although doctors have a huge arsenal of drugs and antibiotics capable of wiping out most bacterial infections, a viral invasion is a tougher proposition. "All along, it's been much easier to produce agents to kill bacteria than to kill viruses," says Professor Brian Tomlinson, a clinical pharmacologist at the Chinese University of Hong Kong (CUHK).

The reason lies in the nature of the pathogens themselves. Bacteria are living organisms that, multiplying unchecked, damage bodily tissue. They can be destroyed by cutting off their life-support systems. Antibiotics defeat bacterial infections by attacking enzymes within the bacteria, allowing the body's immune system to mop them up. Viruses, however, are parasites incapable of reproducing on their own. They're inactive--that is, until they burrow into a host cell, taking over its functions in order to replicate and thereby destroying the host. Inside the body, they become vulnerable to drugs only after they invade a cell, but any treatment may damage the cell as well. And even when scientists develop an effective vaccine or antiviral agent, viruses can suddenly mutate--potentially becoming deadlier and even tougher to eliminate.

A virus's worst enemy is the human immune system. When an unknown pathogen like the new coronavirus invades, the body naturally develops antibodies that can seek out and destroy the interloper. The process takes time, however, and sometimes the system doesn't react fast enough. Science can help with vaccines, which prep the body to recognize and produce antibodies against a particular attacker, such as polio. A vaccine for SARS is under development, but even the most optimistic researchers say it may take more than a year to come up with one that works.

In the meantime, clinicians are working feverishly to fine-tune existing antiviral drugs and treatments in order to render SARS less deadly. At present, about one in every 20 SARS victims dies, usually due to swelling in the lungs, a result of the body's own immune-system response. In Hong Kong, doctors claim they are successfully combating the disease using the antiviral drug ribavirin to inhibit the virus combined with corticosteroids to check an overstimulated immune response. Ribavirin works by interfering with intracellular viral replication, slowing the infection's spread within the body. The problem, as microbiologist Professor John Tam of CUHK points out, is that "if you stop the replication, that means you stop the function of the cell."

Ribavirin's side effects, which include anemia, become dangerous at prolonged high dosages. Moreover, laboratory tests in the U.S. suggest that ribavirin may actually do nothing to the coronavirus. Scientists are exploring other antivirals--such as interferon, which boosts the immune system--or even HIV drugs--such as protease inhibitors, which block an enzyme the virus needs to replicate. But too little is known about the coronavirus to predict the effectiveness of these other drugs.

Researchers are even more worried that the coronavirus, which may be a mutated version of a virus common to animals, could mutate again, becoming more resistant to current treatments. "We are beginning to see patients not responding," says Tam, "and that's a very worrying development." A shape shift in the coronavirus' genetic code can make it more virulent and contagious. Highly mutable HIV continues to frustrate doctors, as it transforms before a vaccine can be developed.

Fortunately, the coronavirus seems to be more stable than HIV, and researchers are confident that SARS-specific antivirals and vaccines can be developed over time. For those patients already under attack from a microbe science is only beginning to understand, that help may be too little, too late.